ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
Neural basis of benzodiazepine reward: requirement for α2 containing GABAA receptors in the nucleus accumbens.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- No Abuse Potential of Silexan in Healthy Recreational Drug Users: A Randomized Controlled Trial.The international journal of neuropsychopharmacology · 2021Trial
- Effects of Micronized Progesterone in Menopausal Hormone Replacement Therapy on Sleep.The journal of obstetrics and gynaecology research · 2026Article
- Benzodiazepine Dependence: Clinical and Molecular Aspects, Preventive Strategies and Therapeutic Approaches.International journal of molecular sciences · 2026Review
- Non-Opioid Anesthetics Addiction: A Review of Current Situation and Mechanism.Brain sciences · 2023Review
- Midazolam, methamphetamine, morphine and nicotine intake in high-drinking-in-the-dark mice.Addiction biology · 2022Article
- GABAFrontiers in psychiatry · 2022Review
- Article
- Evaluation of the anti-conflict, reinforcing, and sedative effects of YT-III-31, a ligand functionally selective for α3 subunit-containing GABAJournal of psychopharmacology (Oxford, England) · 2020Article
- Looking for Novelty in an "Old" Receptor: Recent Advances Toward Our Understanding of GABAFrontiers in neuroscience · 2020Review
- An Emerging Circuit Pharmacology of GABATrends in pharmacological sciences · 2018Review
- Valium without dependence? Individual GABANeuropsychiatric disease and treatment · 2018Review
- Role of GABAMolecular brain · 2017Review
- Further evaluation of the potential anxiolytic activity of imidazo[1,5-a][1,4]diazepin agents selective for α2/3-containing GABAPharmacology, biochemistry, and behavior · 2017Article
- Pharmacological and antihyperalgesic properties of the novel α2/3 preferring GABABrain research bulletin · 2017Article
- A Pharmacogenetic 'Restriction-of-Function' Approach Reveals Evidence for Anxiolytic-Like Actions Mediated by α5-Containing GABAA Receptors in Mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- The Role of Benzodiazepines in the Treatment of Epilepsy.Current treatment options in neurology · 2016Article
- Negative allosteric modulation of GABAA receptors inhibits facilitation of brain stimulation reward by drugs of abuse in C57BL6/J mice.Psychopharmacology · 2016Article
- Antagonism of triazolam self-administration in rhesus monkeys responding under a progressive-ratio schedule: In vivo apparent pA2 analysis.Drug and alcohol dependence · 2016Article
- α2-containing GABA(A) receptors: a requirement for midazolam-escalated aggression and social approach in mice.Psychopharmacology · 2015Article
- Analgesia and unwanted benzodiazepine effects in point-mutated mice expressing only one benzodiazepine-sensitive GABAA receptor subtype.Nature communications · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Despite long-standing concerns regarding the abuse liability of benzodiazepines, the mechanisms underlying properties of benzodiazepines that may be relevant to abuse are still poorly understood. Earlier studies showed that compounds selective for α1-containing GABAA receptors (α1GABAARs) are abused by humans and self-administered by animals, and that these receptors may underlie a preference for benzodiazepines as well as neuroplastic changes observed in the ventral tegmental area following benzodiazepine administration. There is some evidence, however, that even L-838, 417, a compound with antagonistic properties at α1GABAARs and agonistic properties at the other three benzodiazepine-sensitive GABAA receptor subtypes, is self-administered, and that the α2GABAARs may have a role in benzodiazepine-induced reward enhancement. Using a two-bottle choice drinking paradigm to evaluate midazolam preference and an intracranial self-stimulation (ICSS) paradigm to evaluate the impact of midazolam on reward enhancement, we demonstrated that mice carrying a histidine-to-arginine point mutation in the α2 subunit which renders it insensitive to benzodiazepines (α2(H101R) mice) did not prefer midazolam and did not show midazolam-induced reward enhancement in ICSS, in contrast to wild-type controls, suggesting that α2GABAARs are necessary for the reward enhancing effects and preference for oral benzodiazepines. Through a viral-mediated knockdown of α2GABAARs in the nucleus accumbens (NAc), we demonstrated that α2 in the NAc is necessary for the preference for midazolam. Findings imply that α2GABAARs in the NAc are involved in at least some reward-related properties of benzodiazepines, which might partially underlie repeated drug-taking behavior.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.